title: Bronchial neutrophilia in patients with noninfectious status asthmaticus.
abstract: Cellular events that occur in status asthmaticus (SA) remain poorly investigated. Autopsy studies frequently emphasized about the presence of eosinophils in bronchial airway wall, whereas recent studies reported increased number of neutrophils in patients dying of sudden-onset fatal asthma. Mucus plugs occluding the bronchial lumen are almost constant features during SA. Bronchial lavage (BL) may be useful to remove mucus plugs in cases of atelectasis and/or refractory SA. We investigated the contribution of different cell types and cellular mediators (neutrophil elastase, eosinophil cationic protein [ECP], histamine, interleukin-8 [IL-8]) to the pathogenesis of SA. We studied 16 BL from eight patients undergoing mechanical ventilation (MV) for SA (time interval from onset of MV = Day 0 to Day 11), four BL from patients undergoing MV without preexisting respiratory disease (V), 11 BL from patients with stable asthma (A) and eight BL from healthy controls (C). SA exhibited higher number and percentage of neutrophils (81.5 +/- 4.5%) than V (44.3 +/- 12.2) (p < 0.05), A (6.9 +/- 2.7) and C (9.5 +/- 3.8) (p < 0.0001), and higher number of eosinophils than V, A, and C (p < 0.01). Neutrophil elastase, ECP, and IL-8 levels were dramatically increased in SA. Histamine was higher in SA than in C and V (p < 0.05). Bronchial neutrophilia was not related to concomitant bacterial infection as bacteriological cultures were positive in only three BL. Eosinophils, mast cells and histamine were higher in BL performed within the first 48 h of MV (p < 0.05) than in BL performed later on. Our results indicate that bronchial inflammation in SA differs from bronchial inflammation in mild asthma. Persistent bronchial neutrophilia is associated with increased eosinophils and mast cells in the early phase of SA. Neutrophils may result in tissue damage and participate to the shedding of the epithelium in SA.
authors.affiliation: Clinique des Maladies Respiratoires, Hôpital A. Calmette, CHRU, Lille, France.
authors.forename: C
authors.initials: C
authors.lastname: Lamblin
authors.forename: P
authors.initials: P
authors.lastname: Gosset
authors.forename: I
authors.initials: I
authors.lastname: Tillie-Leblond
authors.forename: F
authors.initials: F
authors.lastname: Saulnier
authors.forename: C H
authors.initials: CH
authors.lastname: Marquette
authors.forename: B
authors.initials: B
authors.lastname: Wallaert
authors.forename: A B
authors.initials: AB
authors.lastname: Tonnel
mesh_terms: D000328:Adult; D000368:Aged; D001798:Blood Proteins / Q000378:metabolism; D001980:Bronchi / Q000473:pathology*; D001992:Bronchoalveolar Lavage Fluid / Q000166:cytology; D047091:Eosinophil Granule Proteins; D005260:Female; D006632:Histamine / Q000378:metabolism; D006801:Humans; D018836:Inflammation Mediators / Q000378:metabolism; D016209:Interleukin-8 / Q000378:metabolism; D019272:Leukocyte Elastase / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D009504:Neutrophils / Q000473:pathology*; D012121:Respiration, Artificial; D012131:Respiratory Insufficiency / Q000209:etiology; D012141:Respiratory Tract Infections / Q000150:complications; D012260:Ribonucleases; D013224:Status Asthmaticus / Q000150:complications / Q000382:microbiology / Q000473:pathology*
chemical_list: D001798:Blood Proteins; D047091:Eosinophil Granule Proteins; D018836:Inflammation Mediators; D016209:Interleukin-8; D006632:Histamine; D012260:Ribonucleases; D019272:Leukocyte Elastase